Background: EUS response assessment in patients with locally advanced esophageal cancer undergoing neoadjuvant chemoradiation therapy (CRT) is limited by disintegration of the involved anatomic structures.
Objective: Predictive and prognostic values of a prospectively defined maximum tumor thickness (MTT).
Design: Prospective open-label phase ll study (SAKK 75/02).
Curr Opin Gastroenterol
July 2008
Purpose Of Review: This review summarizes recent progress on endoscopic diagnosis and treatment of esophageal high-grade intraepithelial neoplasia and early adenocarcinoma and critically analyzes the literature in the context of preexisting scientific data.
Recent Findings: Narrow band imaging and computed virtual chromoendoscopy enhanced visualization of the mucosal morphology. The type of mucosal and capillary patterns seen on narrow band imaging predicted the presence of specialized intestinal metaplasia, high-grade intraepithelial neoplasia and early adenocarcinoma.
Multiple treatment guidelines for nonsteroidal anti-inflammatory drugs (NSAIDs) suggest that patients with one or more risk factors for NSAID-related ulcer complications should be prescribed preventive strategies such as acid-suppressive drugs, misoprostol or COX-2-specific inhibitors to reduce their risk of serious ulcer complications. However data are lacking as to how many patients have been on preventive measures in accordance to the National Institute for Clinical Excellence (NICE) criteria in our population. We therefore evaluated the extent to which patients with acute gastrointestinal bleeding have been under ulcer-preventive strategies at the time of hospital entry.
View Article and Find Full Text PDFThe chylomicronemia syndrome is well recognized as a rare etiologic factor of acute pancreatitis; however, whether hypertriglyceridemia can cause chronic pancreatitis (CP) remains unclear. We describe the long-time course of 2 brothers with the familial chylomicronemia syndrome caused by identical compound heterozygous mutations in the lipoprotein lipase (LPL) gene with markedly reduced LPL activity. Other etiologic factors were excluded, including mutations in the PRSS1, SPINK1, and CFTR gene.
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